Thursday, July 25, 2013

The Perception of the Facts in the Zimmerman Trial


The New Yorker



Daily Comment


July 16, 2013

The Facts in the Zimmerman Trial


toobin-zimmerman.jpg

Here’s a hypothetical about the George Zimmerman trial. Imagine that all the evidence is unchanged, with one exception. Suppose there was a dog walker who came upon Zimmerman’s confrontation with Trayvon Martin, saw the whole thing, and testified before the jury. Who threw the first punch? Who was the aggressor? Which one of the two shouted for help? Presumably, all those mysteries would be solved. The facts wouldn’t change, but our understanding of them might be entirely different.

The facts matter, and trials are all about facts. Every time there is a high-profile trial, observers rush to draw conclusions about the American legal system—or even about American society—based on the results. But the idiosyncrasies of the trial process generally make such judgments unwise. A dog walker, a security camera, a clearer audio on a 911 tape—and we’d be having a very different conversation about the Zimmerman trial.

The conclusions almost tell more about the observers than about the underlying facts. Consider, for example, one of the critical pieces of evidence in the case—Zimmerman’s call reporting his sighting of Trayvon Martin. It turns out that the call is open to a variety of interpretations.

On the night of February 26, 2012, Zimmerman was patrolling the Retreat at Twin Lakes, a town-house development in Sanford, Florida. At 7:09 P.M., Zimmerman called the non-emergency police-response line. (He did not call 911.) Was he inside or outside of his car at that point? It’s not clear. The range of his observations suggests that he was outside, but he also says that it’s raining. Since you can’t hear any rain on the call, it might mean that he’s still inside the vehicle. (A sound that might be a door chime raises the possibility that he got out of the car during the call.) The fact of the call alone presents different avenues for interpretation. Zimmerman was conducting a neighborhood watch. Does that mean he was a frustrated, wannabe cop? Or does that mean he was a good citizen trying to help a community that was beset by break-ins?

The call begins with Zimmerman reporting a suspicious person walking around in the rain. Zimmerman says, “We’ve had some break-ins in my neighborhood, and there’s a real suspicious guy.” He describes an unknown male “just walking around looking about” in the rain and says, “This guy looks like he is up to no good or he is on drugs or something.” Almost immediately, the dispatcher asks (Zimmerman does not volunteer the information) the subject’s race, and Zimmerman answers, “Black.” In a later observation during the call, Zimmerman confirms that the person is black. Zimmerman reports that the person has his hand in his waistband and is walking around looking at homes. Zimmerman says, further, “These assholes, they always get away.”

The dispatcher appears at first to be asking Zimmerman to keep an eye on the person. “Just let me know if this guy does anything else,” he says. A little later, Zimmerman says, “He’s running.” (Does the fact that Martin was running suggest that he was up to no good, or does it suggest that the young man was running away from Zimmerman?) The dispatcher asks, “He’s running? Which way is he running?” Again, this is an important point. It’s the dispatcher asking (for a second time) Zimmerman to watch the person.

At this point, Zimmerman follows Martin, eventually losing sight of him. The dispatcher asks, “Are you following him?” When Zimmerman answers, “Yeah,” the dispatcher says, “We don’t need you to do that.” Zimmerman responds, “O.K.” This is probably the best-known part of the exchange. The dispatcher says don’t follow him, one theory goes, Zimmerman does anyway, and that causes the fatal confrontation. But this view of the facts obscures the earlier part of the call—when the dispatcher appears to be asking Zimmerman to follow and report the person’s movements. The call ends when Zimmerman gives the dispatcher information about how the police should find him (Zimmerman, that is) in the complex. Zimmerman asks that the police call him upon their arrival so he can provide his location. Zimmerman ends the call at 7:13 P.M. The first police officer arrived on the scene at 7:17 P.M., by which time Trayvon Martin was already dead.

We’ll probably never know with absolute certainty what happened during those four (or so) critical minutes. But how people see the evidence of what happened—then and elsewhere, in this case and others—probably says more about them than about the evidence itself.

Photograph by Gary Green/The Orlando Sentinel/Getty.

Wednesday, July 24, 2013

Criminal jury verdicts aren't really unanimous



Criminal jury verdicts aren't really unanimous: Implications for your practice

The Worst Kept Secret in Criminal Law

We all knew it. Right? There are lots of reasons why individual jurors vote with their peers despite misgivings. They want to be liked. They want to go home. They are tired of being brow-beaten by the others. They don't want to disappoint the judge by hanging the jury. They just don't care. What we didn't know was just how often it happened -- until now.

The statistic previously cited in the debate about the desirability and/or practicality of unanimity was hung jury rates. You've read my discussion of hung jury rates in this very blog. The estimate of the national average is between 6% and 7% of criminal trials end in a hung jury. For felony trials in some California counties, the rate is over 20%. In Oregon, which uses 10-2 verdicts, the rate is below 1%. The problem, of course, is that the hung jury rate is a very poor proxy for what we really wanted to know: How often do juries remain "deadlocked" after completing deliberations? (where deadlock refers to a situation where a unanimous consensus about the right verdict has not been reached).

Nicole Waters of the National Center for State Courts and Valerie Hans of Cornell Law School have finally taken a step towards answering this important question. As part of the National Center for State Courts project on hung juries, the authors gave out post-trial surveys to almost 4000 jurors across 4 states and got back completed forms from almost 3500. This covered 367 trials. Among the questions they asked was: "If it were entirely up to you as a one-person jury, what would your verdict have been in this case?" It is important to appreciate that all of these verdicts were unanimous, in that all the jurors officially voted for it. Therefore, each "conforming dissenter" (Authors' term) is someone who voted for a verdict she thought was wrong.

The Non-Unanimous Bombshell

Remember that estimates of hung jury rates range around 7%. These are the cases with a dissenter who refused to conform. In the Waters and Hans study, 38% of juries contained at least one juror who disagreed with the general outcome of the case but voted for it anyway (conviction or acquittal). This is the most conservative measure of dissent. Juries are often faced with multiple charges against the defendant or a choice among lesser-included-offenses. So, it is possible that a defendant can be convicted, but not of the charge that a juror thought was most appropriate. Taking this into account, 54% of juries contained at least one juror who disagreed with the jury's verdict on at least one charge. That is, more than half of the juries contained at least one juror who voted insincerely. Nearly half of the juries (46%) contained at least one juror who disagreed with the verdict for the most serious charge facing the defendant.

According to the authors, only 82 of 351 dissenting jurors ultimately hung their juries. The article suggests that the average number of dissenters for cases resulting in a hung jury was just over 3. Therefore, we can tease out that about 25 of these cases resulted in a hung jury, or about 7% of the sample (consistent with previous estimates). By contrast, there were typically about 1.5 conforming dissenters on any case that returned a verdict (if there were any conforming dissenters at all). So, for every single hung jury, there were approximately 8 cases in which the purported unanimous verdict was a farce. When debating the merits of unanimity in the future, hopefully scholars and pundits can move beyond the misleading metric of hung jury rates and focus on the real problem at hand: How do we feel about a system that forces jurors to compromise their own values and judgments to conform to the majority will?

Making use of these results in your next case

While we wait for the Supreme Court and the state legislatures to figure out what to do with these revelations (probably nothing), you should consider them carefully as you prepare for future cases.

The first lesson is that very few criminal cases result in truly unanimous juries, even after prolonged deliberations. If you are a criminal defense attorney, you should always hammer away at the "personal responsibility" angle of jury service. Remind jurors that each has taken an oath to hear all the evidence and reach a conclusion based on her own wisdom and conscience. Emphasize that the Court would never want any juror to vote for a verdict she did not believe was correct. I would include language about being sympathetic to their plight: "Sometimes peer pressure can be strong. Sometimes it is just easier to go along with everyone else, to avoid conflict, to be cooperative. I recognize any sympathize with these instincts. But just remember that the Court has not tasked you with being accommodating or friendly or cooperative. The Court has tasked you with doing the right thing."

The authors of this study have examined some of the things that lead dissenters to hold their ground and hang the jury, rather than giving in to the majority. The first result, supported elsewhere, is that dissenters who favor acquittal are less likely to switch their votes than are dissenters who favor conviction. So, in a case with substantial support on both sides, an acquittal is much more likely than a conviction. A prosecutor needs to be certain that she will secure a very substantial majority for conviction in order to avoid a hung jury. By contrast, a defense attorney can secure an acquittal, even if a handful of jurors initially favor conviction.

Procedures matter. I have written in my column for Lawyers Weekly USA about the consequences of different methods of taking votes in the jury room. As I predicted in that piece, Waters and Hans discovered that juries that took secret ballots were more likely to have dissenters on them. The logic here is that a dissenter will worry less about sticking out like a sore thumb if she can register her objection in private. A secret ballot also allows potential dissenters to discover whether they have any allies on the jury. There might be three or four jurors who are reluctant to be the only one raising a hand in favor of the minority position. As a result, none of them do. A potential block of dissenters is never discovered. A secret ballot avoids this game of "chicken."

I have previously discussed in The Jury Box the importance of "straw poll timing" for the nature of jury deliberations. Juries that immediately take a vote find themselves embroiled in "verdict-driven" deliberations, while those who delay voting spend more time in the generally superior "evidence-driven" mode of deliberations. After a vote is taken, jurors tend to fall into camps, with spokespersons emerging for each. As a result, fewer jurors participate in discussion and jurors tend to get locked into their views. The Waters and Hans study shows a small but significant effect of early polling of jurors. When a jury takes an early vote, it is more likely that at least one juror will disagree with the final verdict. This is probably because an initial dissenter is more likely to feel "outvoted" than "convinced" if the deliberations devolve into a discussion of how to get everyone to vote the same way -- rather than getting everyone to agree.

If you have a case in which you are advocating what you fear will be the "unpopular" position (thought legally defensible), you would be advised to encourage jurors to vote by secret ballot. While you cannot instruct the jury to vote in a particular way, keep in mind that they have no explicit instructions about procedures. As such, a subtle suggestion in closing can be effective. "I want you all to keep an open mind. As you tear up those little slips of paper to cast your ballots, I hope that you will consider everything my client has said on the stand..."

It is much harder to find a way to suggest that jurors take an early straw poll. In fact, many judges now recommend to juries that they not be in a hurry to take a vote, first spending a fair amount of time just sorting through the evidence. Remember that an early vote is a two-edged sword. While it might cause your supporters to harden their positions a bit, it also reduces their abilities to sway the votes of jurors on the other side.

One important question is how volatile are juror evaluations of cases. That is, do they generally change their minds during a case? The answer to this question is a bit unclear. Over 62% of jurors indicated that they had changed their minds at least once during their case. But what does a juror mean when she says she "changed her mind"? Given that 40% of conforming dissenters admitted to changing their minds during deliberations, as compared to 25% of holdouts (those who hung their juries), I fear that many respondents equated changing their votes with changing their minds. The percentage of jurors who reported changing their minds at some stage prior to deliberations is closer to 25% (difficult to pinpoint from the reported data). Some of these respondents are undoubtedly reporting an earlier change as a compensatory mechanism for cognitive dissonance -- they don't want to admit to themselves that they were bullied into changing their votes during deliberations. That said, it would seem a conservative estimate that about one in five jurors really does change her evaluation of the case at some point in the proceedings.

The lesson here would seem to be that a case is not really won or loss during jury selection, as many cynics would argue. There are a substantial number of jurors who can be convinced to re-evaluate their initial positions during a trial. So, pay close attention to your trial technique. Make sure your case is coherent and clear. Finally, be sure to hit the high points in closing to reinforce the items that might have gotten jurors rethinking their views.

This brings us to the question of jury selection. It turns out not to be so critical to select a jury fully comprised of your supporters. These juries seem few and far-between. Most cases result in at least some form of disagreement among jurors that must be resolved during deliberations, either through a genuine exchange of ideas or, more likely, the conversion of conforming dissenters. This reinforces something that trial consultants like me have been trying to explain to clients for years. When evaluating a prospective juror, it is important to consider not only whether the juror is likely to be sympathetic to your case, but also what role the juror is likely to play on the jury. If the juror turns out to favor the other side, is she going to be a holdout or a conforming dissenter? I can't always tell if a prospective juror is going to be pro-prosecution or pro-defense, but I usually have a good sense about whether she is likely to be a leader or a follower, whether she seems more eager to please the court or those around her, whether she relishes the opportunity to be a contrarian. These characteristics are critical and must be explored during jury selection.

OK. This post is really, really long. That's because I think these results are really, really important. Among other things, they emphasize the importance of relying on data, not conjecture. Those who presumed that unanimous verdicts were produced by unanimous juries are just dead wrong. What else might they be wrong about? Do you really want to rely on conjecture the next time you need to pick a jury, or prepare a witness, or select a trial theme? There is no substitute for good research. OK, there's my quick sales pitch.

Please comment on this post! Let's see if we can stir up some trouble.

Sunday, July 21, 2013

Neuroplasticity, Psychosocial Genomics, and the Biopsychosocial Paradigm in the 21st Century

NIH Public Access Header

Health Soc Work. Author manuscript; available in PMC 2010 September 6.
Published in final edited form as:
Health Soc Work. 2009 August; 34(3): 191–199.
PMCID: PMC2933650
NIHMSID: NIHMS217651

Neuroplasticity, Psychosocial Genomics, and the Biopsychosocial Paradigm in the 21st Century

Eric Garland, Ph.D., LCSW
College of Social Work Florida State University Tallahassee, FL 32308
Matthew Owen Howard, Ph.D., Frank Daniels Distinguished Professor of Social Policy

Abstract

The biopsychosocial perspective is a foundation of social work theory and practice. Recent research on neuroplasticity and psychosocial genomics lends compelling support to this perspective by elucidating mechanisms through which psychosocial forces shape neurobiology. Investigations of neuroplasticity demonstrate that the adult brain can continue to form novel neural connections and grow new neurons in response to learning or training even into old age. These findings are complemented by the contributions of psychosocial genomics, a field of scientific inquiry that explores the modulating effects of experience on gene expression. Findings from these new sciences provide external validation for the biopsychosocial perspective and offer important insights into the manifold means by which socioenvironmental experiences influence neurobiological structure and function across the life course.
Keywords: biopsychosocial, neuroplasticity, psychosocial genomics, gene-environment interaction

Introduction

Social work professionals in the 21st Century have adopted the biopsychosocial paradigm. This paradigm, first articulated by the physician, George Engel, holds that humans are dynamic systems whose functioning depends on the holistic integration of biological, psychological, and social factors (Engel, 1977); indeed, according to the biopsychosocial model, these factors are fundamentally interrelated and interdependent. Although Engel rejected the reductionism of the dominant biomedical model of his era, which assumed that molecular biological processes (e.g., genes and biochemistry) immutably dictated physiology and behavior, a simple-minded biological determinism nonetheless took root and became widely, if uncritically, accepted. At its inception, there was scant evidence to support Engel's biopsychosocial perspective; however, scientific discoveries of the past decade have provided important new findings validating and elaborating the biopsychosocial paradigm.

Over the past decade, two fields of empirical investigation, neuroplasticity and psychosocial genomics, have offered important findings that may lead to a paradigm shift in our conceptions of psyche and soma and the modes of their interrelationships. These two fields mutually inform one another, depicting interpenetrating biopsychosocial relationships on different scales: 
neuroplasticity research describes how neurons within the brain proliferate and grow new connections across the lifespan, whereas psychosocial genomics describes the processes by which psychological and social experiences activate or deactivate genes, thereby driving the development of new neural pathways. 
The interplay of these sciences reflects a vision of humans as inherently resilient; psychosocial factors appear to stimulate gene expression within neurons resulting in alterations to the structure and function of the brain. Discoveries from both fields reveal that experience and learning can contribute to positive change, even at the neurobiological and structural levels.

Social work academicians have embraced the biopsychosocial perspective; yet, many are perhaps not fully aware of recent developments in genomic and neurobiological research with implications for social work and the biopsychosocial perspective. This research provides insights into the very substrates of biopsychosocial change. Thus, we review recent neuroplasticity and psychosocial genomics research and its implications for current understanding and application of the biopsychosocial perspective.

Neuroplasticity

Basic neurotransmission

The human brain is a complex, self-organizing, biological system, consisting of trillions of interconnected nerve cells called neurons. The operation of neurons results in two distinct forms of information processing: signaling and integration. Each neuron propagates signals via action potentials, electrochemical currents that travel the length of its axon. This current leads to the release of neurotransmitters which traverse synapses, the gaps between neurons. These chemical messages are received via specialized receptor cells at the ends of numerous, tree-like branches of the receiving neuron, called dendrites. The stimulation of dendritic receptors by neurotransmitters leads to integration, whereby large amounts of information from many neurons is summed up before reaching a threshold to fire the action potential down the next axon. In this manner, perceptual information from the external environment and the internal milieu of the body is transmitted and processed in the brain, leading to cognition, emotion, and behavior, the essence of human experience.

Origins of neuroplasticity research

The brains of infants and children are known to be plastic, undergoing spurts of neuronal development in response to stimulus exposure during critical periods (Mundkur, 2005). This development consists of the genesis of neurons, increased connectivity between extant neurons, and the routing of new synaptic connections between previously unrelated neurons. However, before 1998, it was widely accepted that neuronal connections in the adult brain were immutable; the neurons that populated a given brain area were thought to be fixed in accordance with whatever form and function the genetic code prescribed for that region (Begley, 2006). In addition, the conventional wisdom at the time--that no new neurons could be generated after injury or insult to the brain—was held with conviction on the part of leading neuroscientists.
However, upon discovery of the growth of new neural tissue, or neurogenesis, in the adult human hippocampus, a brain region responsible for memory (Eriksson et al., 1998), the dogma of the “hardwired brain” was formally repudiated. This finding complemented earlier evidence from primate studies demonstrating that novel sensory experience and learning new behaviors triggers neuronal growth in the somatosensory and motor cortices, areas of the brain subserving tactile perception and limb movement (Jenkins, Merzenich, Ochs, Allard, & Guic-Robles, 1990; Nudo, Milliken, Jenkins, & Merzenich, 1996). Subsequent to the discovery of neurogenesis in the adult human brain, neuroscience has pursued this line of investigation with vigor, aided by advances in brain imaging techniques such as magnetic-resonance imaging.

Neuroplasticity research findings

The growth of neurons has been documented in the brains of adults exposed to a variety of experiences. For instance, violinists evidence neural growth in the portion of their somatosensory cortex devoted to their fingering hand through hours of musical practice (Elbert, Pantev, Wienbruch, Rockstroh, & Taub, 1995), as do persons engaged in the practice of juggling (Draganski et al., 2004). In addition to such physical training, mental practice may promote neuroplasticity: neurogenesis can occur in the motor cortex just by imagining playing the piano (Pascual-Leone, Amedi, Fregni, & Merabet, 2005). Similarly, taxicab drivers develop the areas of their brains involved in spatial relationships by memorizing the labyrinthine streets and avenues of the cities in which they work (Maguire et al., 2000). While the underlying mechanisms are different, neuroplasticity research suggests that challenging learning experiences can lead to the development of brain tissue analogous to the way physical exercise can lead to the development of muscle tissue.

One area of research that has found significant evidence of mental training leading to neuroplastic modifications in brain activity focuses on the study of meditation. Meditation, while greatly varying in technique and purpose across the diverse spiritual and cultural traditions where it is employed, may be generally defined as the intentional practice whereby one grasps “the handle of cognition” to cultivate a competent use of his or her own mental capacities, gaining agency over thought and emotion (Depraz, Varela, & Vermersch, 2003). Such intentional mental training has been shown to induce functional neurobiological changes.

A study by Lutz and colleagues found marked alterations in the synchronization of neurons as an effect of long-term training in Buddhist loving-kindness meditation, a practice which is thought by some practitioners to promote a state of unconditional compassion and benevolence (Lutz, Greischar, Rawlings, Ricard, & Davidson, 2004). Neural synchrony of the type observed in this study may be indicative of coherent and integrated psychological functioning (Williams et al., 2005). The synchronization of brain activity found in some of the practitioners sampled, whose experience ranged between 10,000 and 50,000 hours spent in meditation, was higher than any previously reported in the literature. Such increased neural synchrony was observed not only during the meditative state, but also when the practitioners were not meditating, suggesting that long-term mental practice can induce lasting, trait-level changes possibly mediated by structural modifications to the brain (Begley, 2006).

Other research has documented changes in neurobiological function as a result of mindfulness meditation, the practice of cultivating a present-centered, metacognitive awareness, “a naturalistic state wherein consciousness transcends its content to rest upon the dynamics of its own processes” (Garland, 2007). A recent study by Slagter et al. (2007) compared attentional performance of a group of experienced meditators participating in a 3-month mindfulness meditation retreat to that of a novice control group who received a 1-hour meditation class and were asked to meditate 20 minutes daily for one week. Relative to controls, experienced meditators evidenced significant improvements in attentional performance that correlated with alterations in brain activity. This cognitive enhancement was maintained 3 months after formal meditation practice, providing suggestive evidence that mental training can stimulate neuroplastic changes in the adult human brain (Slagter et al., 2007).

While the work of Slagter et al. and Lutz et al. provide tentative support for meditation-induced neuroplasticity, neither study examined structural brain changes per se. However, two structural MRI investigations comparing the brains of experienced meditators to control subjects matched in sex, age, race, and years of education found that years of meditation experience correlated with increased cortical thickness in brain areas where visceral attention (e.g. right anterior insula) and self-awareness (e.g. left superior temporal gyrus) have been localized (Holzel et al., 2008; Lazar et al., 2005). These empirical investigations of meditation suggest that mental training may stimulate structural alterations reflective of neuroplasticity.

Clinical implications of neuroplasticity research

The finding that experience and training can lead to the development of new neural connections has key implications. For example, persons suffering from what was once thought to be permanent brain injury can heal through rehabilitation designed to stimulate the damaged area, such as in the case of stroke (Taub et al., 2006). However, although largely speculative, it is possible that neuroplasticity may undergird not only rehabilitation of physical illness but that of select psychological disorders as well, mediating natural recovery from mental illness in some cases as well as improvements related to psychosocial interventions. At present, it has been demonstrated that psychotherapy can induce functional changes in brain activation. For example, a brain imaging study found that persons with obsessive-compulsive disorder who were treated with a mindfulness-oriented form of cognitive-behavioral therapy (CBT) exhibited functional changes in the orbital frontal cortex and striatum, two brain structures found to be overactive in OCD (Schwartz & Begley, 2002). Other studies have demonstrated psychotherapy-related alterations in brain circuits involved in depression (e.g. Goldapple et al., 2004; Martin, Martin, Rai, Richardson, & Royall, 2001). CBT has also been associated with changes in frontal and temporal brain regions of persons suffering from panic disorder (Prasko et al., 2004). Such intervention-related changes in both psychosocial function and neural activity may correlate with neuroplastic alterations to the brain; critically, a combined functional and structural magnetic resonance imaging study of practice-induced increases in gray matter found that increased task-specific brain activation led to the remodeling of one of the same neural structures (i.e. dorsolateral occipital cortex) that was activated by the practice and learning of the task (Ilg et al., 2008).

Neuroplasticity research of psychosocial interventions has just begun. A recent longitudinal study of cognitive-behavioral therapy for women with chronic fatigue syndrome found increases in gray matter of the lateral prefrontal cortex after 16 sessions of CBT (de Lange et al., 2008). Increases in gray matter volume correlated with enhanced cognitive processing speed, suggesting that the neuroplasticity evoked by psychotherapy played a causal role in rehabilitation of cognitive performance after cerebral atrophy resulting from chronic fatigue.

Indeed, neuroplasticity may be the biological mechanism through which psychosocial interventions exert at least some of their therapeutic effects. During psychotherapy, when the client recalls negative or painful life experiences, the clinician may assist in reframing the context so that the experience gains new meaning (de Shazer, 1988). For instance, in treating persons who have experienced traumas such as rape, therapy may help clients to envision themselves as a survivor rather than as a victim. Such reframing or reappraisal may be a critical component of successful biopsychosocial outcomes (Folkman, 1997; Penley, Tomaka, & Wiebe, 2002). Some theorists hypothesize that the process of recalling, reconstructing, and reframing memories of past trauma during psychotherapy is mediated by the reorganization and genesis of neurons (Centonze, Siracusano, Calabresi, & Bernardi, 2005; E.L. Rossi, 2005). This hypothesis is founded on evidence that the formation of new long-term memories results from neuroplastic changes in the brain structure known as the hippocampus. Hippocampal changes appear within hours of significant learning experiences (McGaugh, 2000), such as those that can occur during psychotherapy.

Neuroplasticity is mediated at the cellular level through activity-dependent gene expression, the mechanism by which neurons secrete growth factors leading to the “activation of gene transcription in the nucleus that support[s] synaptic connections…Thus, with every new experience, the brain slightly rewires its physical structure and this rewiring is mediated through the signaling cascade” (Mundkur, 2005). Hence, in order to understand neuroplasticity, we must consider the domain of psychosocial genomics.

Psychosocial Genomics

Basic epigenetics

In the 21st century, there is broad agreement that the genome is the basis of human life and a precondition for psychosocial experience. Nevertheless, the question of the respective roles of nature and nurture in human experience and the manner of their interaction in select contexts remains contentious, despite the more than half-century that has transpired since Watson and Crick (1953) identified DNA as the building block of biological processes.

The DNA code of the human genome does not determine protein synthesis in a one-toone fashion; instead, genes are subject to epigenetic processes (i.e. modifications that do not occur due to changes in the basic genetic sequence of amino acids but that instead result from biological and environmental influences on the expression of genes as proteins) (Eisenberg, 2004). During gene expression, the genetic code serves as a “blueprint” that guides the construction of proteins from amino acids. However, this construction process is modulated by signals from the internal and external environments, which steer and modify the manner in which basic organic molecules are organized into anatomy and physiology. Although genes prescribe protein synthesis, there is substantial variability in the manner in which they are expressed.

A single genotype, the genetic blueprint of an organism, can be expressed in a multiplicity of distinct physiological and behavioral forms, known as phenotypes. This is evident in Eisenberg's (2004) example of phenylketonuria, a disorder that when untreated may lead to severe mental retardation, psychosis, and seizures. If children with this genetic abnormality are kept on a postnatal diet low in the amino acid phenyalanine, they do not develop these disorders. Hence, although the genotype for phenylketonuria does not change, its phenotypic expression is modified by the environment (i.e., nutrition) to which the individual has been exposed. The mechanisms by which such different phenotypes are expressed are just beginning to be understood, but appear to involve the regulatory effect of internal and external environmental signals on stress hormones, which in turn modify gene transcription processes (Kandel, 1998; E. L. Rossi, 2004).

Learning and other psychosocial experiences may modulate gene expression

In addition to physical environmental forces, learning experiences in the social environment can alter gene expression (McCutcheon, 2006). The bi-directional relationship of nature and nurture, genes and environment, was first demonstrated in a series of path-breaking studies of maternal care in rats (Francis, Champagne, Liu, & Meaney, 1999; Liu et al., 1997). In these studies, an inverse relationship was found between the number of stress hormone receptors in a rat's hippocampus and its tendency to exhibit stress reactions. The number of these receptors is dictated by the genotype of the rat. Highly stress-reactive rats give low levels of maternal care to their offspring, who, in turn, exhibit high stress reactivity and later provide low levels of maternal care to their offspring. However, these studies revealed that hormonal and behavioral stress reactions of rat pups as well as the number of their stress hormone receptors are modulated by the licking, grooming, and nursing behaviors of their mothers. Even if a rat were born with a genotype coding for fewer stress hormone receptors, if it was reared by an adoptive mother providing high levels of maternal care, the rat's genes produced more stress receptors, making it calmer, less reactive to stressors, and more apt to provide maternal care to its offspring. These findings offer some evidence that social behavior may be inherited and transduced via gene expression into neuroplastic alterations in brain structure, leading to psychobiological learning and change.

The notion that social experience can lead to changes in gene expression was voiced most prominently by Nobel laureate, Eric Kandel, who regarded this observation as the core component of a new paradigm for psychiatry (1998). Kandel summarized the current state of biological thinking with regard to the relation between social experiences and neurobiology, observing that:
The regulation of gene expression by social factors makes all bodily functions, including all functions of the brain, susceptible to social influences. These social influences will be biologically incorporated in the altered expressions of specific genes in specific nerve cells of specific regions of the brain. These socially influenced alterations are transmitted culturally (Kandel, 1998, p. 461).
This powerful claim, while supported by over a decade of rigorous research, has rarely been directly tested. However, advances in psychoendoneuroimmunology, the study of how mental processes affect the immune system, have clearly shown the effects of psychological and social factors on human physiological functions that indirectly involve the genetic replication of cells (Ray, 2004). Such alterations of biological function may be mediated through experience-dependent gene expression, the process whereby social-environmental signals turn genes “on” and “off,” leading to alterations in protein synthesis which ultimately result in physiological changes (Pinaud, 2004).

Psychosocial genomic hypotheses

Although our genes provide a basic outline for development, environmental influences such as social experiences shape gene expression and ultimately make us unique individuals. This interaction is the essence of what Rossi (2002) has termed “psychosocial genomics,” the interdisciplinary study of the processes by which gene expression is modulated by psychological, social, and cultural experiences. Practitioners might profit from knowing more about this new science, for according to Kandel:
Insofar as psychotherapy or counseling is effective and produces long-term changes in behavior, it presumably does so though learning, through producing changes in gene expression that alter the strength of synaptic connections and structural changes that alter the anatomical pattern of nerve cells of the brain (Kandel, 1998, p. 460)
Thus, it is conceivable that psychosocial interventions, the tools of social work practice, may produce alterations in gene expression leading, in some cases, to measurable neurobiological changes. Since can stress affect neurogenesis through alterations in gene expression and transcription (Glaser et al., 1990; Warner-Schmidt & Duman, 2006), ultimately leading to dysregulation of affect (Post, 1992), psychosocial interventions designed to reduce distress and improve mood may affect brain structure and function through this pathway. Muenke (2008) has recently suggested that the therapeutic effects of stress-reduction techniques might be mediated by changes in gene expression. In line with this hypothesis, a recent study of a meditative breathing practice found increased gene expression of the immune factors glutathione S-transferase, Cox-2, and HSP-70 in practitioners relative to controls (Sharmaa et al., 2008). While this study supports the psychosocial genomic hypothesis, its cross-sectional design does not allow for confident inferences vis-à-vis causality. However, in light of this potential shortcoming, a longitudinal study examined gene expression before and after exposure to eight weeks of meditation training (Dusek et al., 2008), and found alterations in the expression of 1561 genes after the intervention. Among these changes were increases in the expression of genes associated with the stress response, suggesting that learning to engage the relaxation response through meditation may attenuate the deleterious impact of stress on cellular processes.

Although controlled psychosocial genomic research is uncommon, there are a growing number of psychosocial intervention studies that do measure physiological outcomes such as blood levels of cortisol or immune factors. For instance, stress reduction interventions have been shown to increase numbers of immune cells and decrease numbers of cells associated with allergic reactivity (Castes et al., 1999), and improve antibody response to the flu vaccine (Davidson et al., 2003). Intervention-related changes in such biological markers may serve as indirect measures of alterations in gene expression.
The new scientific paradigm outlined above provides a perspective on how the biopsychosocial constitutions of practitioners and clients might interact in the act of therapy:
When a therapist speaks to a patient and the patient listens, the therapist is not only making eye contact and voice contact, but the action of neuronal machinery in the therapist's brain is having an indirect, and, one hopes, long-lasting effect on the neuronal machinery in the patient's brain; and quite likely, vice versa. Insofar as our words produce changes in our patient's mind, it is likely that these psychotherapeutic interventions produce changes in the patient's brain. From this perspective, the biological and sociopsychological approaches are joined. (Kandel, 1998, p. 466)
The union of neuroplasticity and psychosocial genomics research represents a synthesis of the social and biological sciences that is non-reductive: it does not dismiss human experience as the product of a neural machine, pre-determined by its genetic blueprint. Instead, it is integrative, inclusive, and holistic; this unitary approach reveals the power of thought and emotion, society and culture to affect not only our phenomenological experience but our very neurobiological structure and function. In sharp contrast to genetic determinism, this new paradigm envisions individuals as having the innate potential for agency over the tripartite dimensionality of their biopsychosocial selves.

Implications for Social Work

The social work profession's historical emphasis on the social environment as the context for individual well-being is supported by research over the past decade. Neuroplasticity and psychosocial genomic research indicate that socioenvironmental forces have the potency to alter human well-being through their effects on neurobiology. Social experience may be transduced through the activation of neurons, leading to modifications in the phenotypic expression of genes and eventuating in structural changes to the brain. While genes and neurobiology may be the substrates of vulnerability to environmental stressors, they are also, in all likelihood, the substrates of resilience (D Cicchetti, 2003; D. Cicchetti & Blender, 2006).

The sciences of neuroplasticity and psychosocial genomics may provide new empirical bases for social work interventions. Biological measures of change can and should be used to enhance the evaluation of social intervention research. Given the current funding climate and priorities of the National Institutes of Health, research programs designed to evaluate social work practice might be more likely to obtain grant support if interventions studied were evaluated with physiological outcome measures including those assessing gene expression and neuroplasticity. In time, a given practice may be deemed “evidence-based” when, among other criteria, it is shown to result in plastic brain changes or altered gene expression associated with improved biopsychosocial functioning.

Currently, there is a paucity of empirical support for this new paradigm in studies with humans. An abundance of research on higher mammals indicates that experience can trigger gene expression leading to neuroplasticity. As referenced earlier in this paper, several studies on humans indicate that learning and training led to neurogenesis and the reorganization of neural networks. Despite developments in these lines of research, science has only begun to examine the effects of psychosocial interventions on brain structure and function. More research must be conducted in this emerging field, and the social work profession, with its expertise in addressing social problems and enhancing human well-being, can make a vital contribution to this endeavor.
Brain imaging and gene assays may be utilized to detect the neuroplastic and genomic effects of psychosocial interventions. Technologies such as magnetic resonance imaging (MRI), functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) are capable of assessing the neurophysiological changes associated with psychosocial interventions (Kumari, 2006). Reductions in psychiatric symptoms may be reflected in the alterations in brain metabolism and structure revealed by these imaging technologies. DNA microarray technologies, which can evaluate messenger RNA production in cells and thereby determine which genes are activated (Mirnics, Middleton, Lewis, & Levitt, 2001; Raychaudhuri, Sutphin, Chang, & Altman, 2001), have been used to assess alterations in gene expression related to post-traumatic stress disorder (Segman et al., 2005), social aggression (Berton et al., 2006), and depression (Evans et al., 2004). DNA microarrays may become more widely used to measure biological effects of psychosocial interventions in the not-too-distant future (E. L. Rossi, 2005).

Nevertheless, the funding and specialized training necessary to perform brain imaging and DNA microarrays decreases the likelihood that social work researchers working in isolation could leverage these technologies for biopsychosocial research. Consequently, future psychosocial intervention research could involve interdisciplinary teams of social workers, neuroscientists, and molecular biologists, where data from the biological sciences could be complemented by the insights of social work research. Alternatively, other more accessible biological markers, such as stress hormone levels in saliva, could be measured as a proxy for physiological change induced by psychosocial interventions. For example, salivary cortisol assays are a relatively inexpensive form of assessment that can be done by many university laboratories. Social work investigators could add this measure to their intervention research protocols.

Whether the impact of psychosocial interventions can be traced at the neuronal, genomic, or grosser levels of physiological response, biological markers will only be meaningful as a complement to self-report and collateral measures of change. Indeed, Engel's biopsychosocial paradigm is rooted in the philosophical principle of complementarity (Freedman, 1995); instead of the “either/or” mentality of dualistic reductionism, biopsychosocial research should embrace a “both/and” logic, where reports of subjective experience garnered through validated instruments and qualitative interviews are correlated with biological and behavioral data. Such research can add value to Social Work as a primary mental health and allied-health profession and lead to the implementation of interventions with demonstrable physiological, psychological, and behavioral benefits.

Conclusion

Over the past decade neuroplasticity research has enriched the biopsychosocial perspective by demonstrating that psychosocial experiences not only influence neurobiological processes but may actually change the structure of the adult brain. These structural changes consist of increased arborization of neurons, enhanced synaptic connectivity, and even the genesis of new neural tissue. Although neuroplasticity research is in its infancy, recent findings suggest that the effects of psychosocial experiences such learning and mental training on cognitive, emotional, and behavioral functions may be mediated by alterations to the architecture of the brain.

In turn, experience-dependent modifications to neural tissue may be driven by epigenetic processes (i.e., changes in gene expression produced by environmental determinants). The human environment is constantly conditioned by social experiences, which, when transduced by the nervous system into electrochemical signals, may modulate protein synthesis in the nuclei of nerve cells, ultimately leading to changes in the replication and growth of neurons. Social experience can change gene expression, leading to the restructuring of the brain through neuroplasticity. While tentative at present, empirical investigations of the psychosocial genomic hypothesis will likely proliferate over the next decade.

These new biopsychosocial sciences are consistent with a view of human beings as holistic, recursive systems structurally coupled with their environments in a process of mutual change (Maturana & Varela, 1987). Intentionality and volition can generate changes in the structure of the brain, the very organ assumed to produce such mental phenomena (Schwartz & Begley, 2002). With this finding it is evident that human experience is not driven solely from the bottom-up by neurobiology and genetics. Instead, there is growing evidence that psychosocial experience can exert a macrodeterministic, top-down force upon our biology. In the philosophy of emergent interactionism, Roger Sperry, Nobel laureate neuroscientist, described macrodeterminism as a higher-order, molar level of organization that determines and conditions the activity of lower-order, nested sub-components (Sperry, 1987). Hence, human beings, who are at one level assemblies of organ systems comprised of aggregates of cells, in turn composed of organic molecules made up of sub-atomic particles, are not merely the summation of these physical elements. Instead, the consciousness that emerges from the interaction of these components can act back upon its physical substrate. Thought, emotion, and action trigger neural activity, which can lead to a re-organization of the brain, shaping future psychosocial experience. From this perspective, we are not the passive products of neurophysiology and heredity; rather, through our behavior in the social environment, we become active agents in the construction of our own neurobiology, and ultimately, our own lives.

This new paradigm may reveal the empirical foundation of that most central of social work principles, the idea that people have the power to transcend and transform their limitations into opportunities for growth and well-being.

Acknowledgments

ELG was supported by Grant Number T32AT003378 from the National Center for Complementary and Alternative Medicine.

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Tuesday, July 16, 2013

Changes In DSM-5: Racism Can Cause PTSD Similar To That Of Soldiers After War





Changes In DSM-5: Racism Can Cause PTSD Similar To That Of Soldiers After War

Updates to the recently released DSM-5 could potentially transform how race-based traumas are diagnosed in ethnic minorities.


By Nadia-Elysse Harris, JD | May 23, 2013 04:51 PM



Dr. Monnica T. Williams suggests that proposed changes in the criteria for post-traumatic stress disorder (PTSD) in the fifth edition of the Diagnostic Manual of Mental Disorders (DSM-5) could increase the potential for better recognition of race-based trauma in racial and ethnic minorities.

In a recent article in Psychology Today, Williams, who is a clinical psychologist and the associate director of the University of Louisville's Center for Mental Health Disparities, said that before the release of the DSM-5 Thursday, racism was recognized as a trauma that could potentially cause PTSD, but only in relation to a specific event. There had to be an incident of intense fear,
helplessness, or horror for such consideration. For instance, if someone was assaulted in a racially-motivated event, then racism qualified as a sufficient trauma to be categorized as a cause of PTSD.

But now, under the new definition, the requirements for fear, helplessness, and horror have been removed, making room for the more lasting effects of subtle racism to be considered in the discussion of race-based traumas.

In 2011, researchers found that African Americans who reported experiences of racial discrimination had higher odds of suffering from generalized anxiety disorder (GAD). An article on PsychCentral termed the phenomenon as "racial battle fatigue, saying that "exposure to racial discrimination is analogous to the constant pressure soldiers face on the battlefield."

"While the term [racial battle fatigue] is certainly not trying to say that the conditions are exactly what soldiers face on a battlefield, it borrows from the idea that stress is created in chronically unsafe or hostile environments," said Dr. Jose Soto, Ph.D., associate professor of psychology at University of California, Berkeley.

Williams builds on that concept, saying that many minorities experience lasting, cumulative effects of racism that could lead to the development of PTSD. "It was found that in many cases, such as soldiers trained in combat, emotional responses are only felt afterward, once removed from the traumatic setting," she wrote. So, even when experiences aren't immediate and earth-shattering, their effects can have the magnitude to cause long-lasting trauma.

The addition of factors like intrusion symptoms, persistent avoidance, alteration in cognition and mood, and hyperarousal and reactivity to the DSM-5 bode well for the treatment of patients experiencing race-based trauma, according to Williams.

The DSM-5, which is often referred to as the mental health "bible," was released amid skepticism, including an announcement from the National Institute for Mental Health that it will no longer fund research based on DSM clusters.